ABSTRACT The overuse of antibiotics has propelled the spread of antibiotic resistance and inflammatory disorders. Despite this, many people expose their skin to a potent antimicrobial on a near daily basis. This antimicrobial, the metal aluminum, is the active ingredient in antiperspirants. Seemingly innocuous, antiperspirants induce severe ecological shifts (dysbiosis) in the skin microbiome, the communities of microbes that reside on skin. Through repeated exposure, antiperspirants may also cause these communities to develop resistance to aluminum, a possibility of high concern since metal and antibiotic resistance are often linked. As commensals, skin microbes cooperate with the immune system to thwart invading pathogens and suppress inflammation. However, dysbiosis can lead these communities to become pro-inflammatory such as in eczema, and in the context of skin injury, self-contamination with commensals can lead to antibiotic-resistant infections such as chronic wounds. How antiperspirants influence these disease functions of skin commensals is unknown. This proposal?s central hypothesis is that aluminum drives antibiotic resistance and pro-inflammatory dysbiosis in the skin microbiome. Recently, metabolic products (metabolites) have been recognized as strong modulators of microbial virulence and host inflammation, suggesting therapeutic applications. Thus, different aspects of the hypothesis will be addressed as follows: (1) determine how aluminum selects for antibiotic resistance in skin commensals, (2) discover metabolites for treating wounds infected with aluminum-resistant skin commensals, (3) discover metabolites for treating aluminum-induced dysbiosis, inflammation, and pathogen invasion. This proposal may reveal how a routinely used antimicrobial product contributes to skin inflammation and the spread of antibiotic resistance.